Linoleic Acid Activates GPR40/FFA1 and Phospholipase C to Increase [Ca2+]i Release and Insulin Secretion in Islet Beta-Cells
中国医学科学杂志(英文版)2012年第1期 页码:18-23
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Linoleic Acid Activates GPR40/FFA1 and Phospholipase C to Increase [Ca2+]i Release and Insulin Secretion in Islet Beta-Cells
Affiliations:
Department of Endocrinology and Metabolism, Fourth Affiliated Hospital , China Medical University,Shenyang,China,110034
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网络出版日期:2012-03-30,
纸质出版日期:2012
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Yi-jun Zhou, Yu-ling Song, Hui Zhou, 等. Linoleic Acid Activates GPR40/FFA1 and Phospholipase C to Increase [Ca2+]i Release and Insulin Secretion in Islet Beta-Cells[J]. 中国医学科学杂志(英文版), 2012,(1):18-23.
Yi-jun Zhou, Yu-ling Song, Hui Zhou, et al. Linoleic Acid Activates GPR40/FFA1 and Phospholipase C to Increase [Ca2+]i Release and Insulin Secretion in Islet Beta-Cells[J]. Chinese medical sciences journal, 2012, (1): 18-23.
Yi-jun Zhou, Yu-ling Song, Hui Zhou, 等. Linoleic Acid Activates GPR40/FFA1 and Phospholipase C to Increase [Ca2+]i Release and Insulin Secretion in Islet Beta-Cells[J]. 中国医学科学杂志(英文版), 2012,(1):18-23.DOI:
Yi-jun Zhou, Yu-ling Song, Hui Zhou, et al. Linoleic Acid Activates GPR40/FFA1 and Phospholipase C to Increase [Ca2+]i Release and Insulin Secretion in Islet Beta-Cells[J]. Chinese medical sciences journal, 2012, (1): 18-23.DOI:
Linoleic Acid Activates GPR40/FFA1 and Phospholipase C to Increase [Ca2+]i Release and Insulin Secretion in Islet Beta-Cells
ObjectiveTo elucidate GPR40/FFA1 and its downstream signaling pathways in regulating insulin secretion. Methods GPR40/FFA1 expression was detected by immunofluorescence imaging. We employed linoleic acid (LA)
a free fatty acid that has a high affinity to the rat GPR40
and examined its effect on cytosolic free calcium concentration ([Ca
2+
]
i
) in primary rat β-cells by Fluo-3 intensity under confocal microscopy recording. Downregulation of GPR40/FFA1 expression by antisense oligonucleotides was performed in pancreatic β-cells
and insulin secretion was assessed by enzyme-linked immunosorbent assay. Results LA acutely stimulated insulin secretion from primary cultured rat pancreatic islets. LA induced significant increase of [Ca
2+
]
i
in the presence of 5.6 mmol/L and 11.1 mmol/L glucose
which was reflected by increased Fluo-3 intensity under confocal microscopy recording. LA-stimulated increase in
[Ca
2+
]
i
and insulin secretion were blocked by inhibition of GPR40/FFA1 expression in β-cells after GPR40/FFA1-specific antisense treatment. In addition
the inhibition of phospholipase C (PLC) activity by U73122
PLC inhibitor
also markedly inhibited the LA-induced [Ca
2+
]
i
increase. Conclusion LA activates GPR40/FFA1 and PLC to stimulate Ca
2+
release
resulting in an increase in [Ca2+]
i
and insulin secretion in rat islet β-cells.
Abstract
ObjectiveTo elucidate GPR40/FFA1 and its downstream signaling pathways in regulating insulin secretion. Methods GPR40/FFA1 expression was detected by immunofluorescence imaging. We employed linoleic acid (LA)
a free fatty acid that has a high affinity to the rat GPR40
and examined its effect on cytosolic free calcium concentration ([Ca
2+
]
i
) in primary rat β-cells by Fluo-3 intensity under confocal microscopy recording. Downregulation of GPR40/FFA1 expression by antisense oligonucleotides was performed in pancreatic β-cells
and insulin secretion was assessed by enzyme-linked immunosorbent assay. Results LA acutely stimulated insulin secretion from primary cultured rat pancreatic islets. LA induced significant increase of [Ca
2+
]
i
in the presence of 5.6 mmol/L and 11.1 mmol/L glucose
which was reflected by increased Fluo-3 intensity under confocal microscopy recording. LA-stimulated increase in
[Ca
2+
]
i
and insulin secretion were blocked by inhibition of GPR40/FFA1 expression in β-cells after GPR40/FFA1-specific antisense treatment. In addition
the inhibition of phospholipase C (PLC) activity by U73122
PLC inhibitor
also markedly inhibited the LA-induced [Ca
2+
]
i
increase. Conclusion LA activates GPR40/FFA1 and PLC to stimulate Ca